The PR-10 proteins are the most important family of PR proteins associated with pollen-food allergy syndrome. The major birch allergen Bet v 1 is a member of this family of proteins. Birch was one of the first pollen allergies associated with hypersensitivity to various fruits and vegetables.56 A major antigenic protein in apples, Mal d 1, cross-reacts with Bet v 1 (Table 1, 5). Other fruits and vegetables with homologous proteins to Bet v 1 include the following: cherry, apricot, pear, peach, hazelnut, celery, carrot, parsley, and potato (Table 1, 2, 5).28,43 Consumption of these foods in birch-allergic individuals can lead to the symptoms of OAS. Patients with atopic dermatitis who are sensitized to birch pollen may experience a worsening of their eczema after consumption of birch pollen–related foods.57,58 Oropharyngeal reactions caused by foods that are related to birch pollen are more prevalent in central and northern Europe where birch trees are common.59
Lipid transfer proteins comprise the PR-14 family of proteins and can be found in tomatoes, peaches, apples, apricot, plum, cherry, almonds, and grapes.28,60 Lipid transfer proteins are cross-reacting antigens responsible for OAS triggered by consumption of apples and peaches in patients without birch or grass pollen allergy.28 Art v 3, the mugwort pollen LTP, has been shown to cross-react with peach LTP Pru p 3 and is involved in the mugwort/peach-associated allergy (Table 1, 2, 5).3 However, this family of proteins may also cause allergy to fruits in the absence of pollen allergy.61 The LTP microarray immunoassay data suggest that peach LTP (Pru p 3) acts as the principal primary sensitizer of food-pollen allergies and as the main gateway to polysensitization to LTPs.50 Lipid transfer proteins are particularly heat-stable and resistant to digestive enzymes, unlike most allergens causing OAS.12,62,63 Stability allows the allergen to reach the gastrointestinal immune system in an immunogenic and allergenic conformation, allowing sensitization and induction of systemic symptoms.64 Consequently, this family of proteins is more likely to cause severe systemic reactions, including urticaria, angioedema, dyspnea, and anaphylaxis.12,28,51,65 The conserved IgE-binding conformation is probably the most important factor contributing to the observation that LTP-reactive patients have a higher incidence of severe systemic reactions than classic birch-related food allergic proteins.61 Often, severe allergic reactions to LTP food allergens are triggered by physical exercise and nonsteroidal anti-inflammatory medications.51 Lipid transfer proteins are dominant allergens in the Mediterranean region and cause severe and systemic symptoms in this region at a higher rate than seen in central Europe.3,59,66
The PR-5 group of proteins has been recognized as a fairly new family of cross-reactive allergens.67 Allergens within the PR-5 group of proteins share homology with thaumatins, intensely sweet proteins first isolated from the tropical plant Thaumatococcus daniellii, native to West Africa.67 Mal d 2, the minor allergen of apple, was the first TLP described as a plant food allergen.68 Pru av 269 (a major allergen of cherry), Cup a 370 (from Cupressus arizonica pollen), Jun a 371 (from mountain cedar), and Man z TLP267 (from sapodilla plum) have also been shown to be homologous to the TLPs (Table 5). Further research is needed to understand the cross-reactivity of TLPs with other foods and pollens.
Profilin, an actin-binding protein ubiquitously present in eukaryotic cells, has also been associated with pollen- and plant-associated food allergies.72 The prevalence of skin sensitization to date-pollen-profilin has been estimated to be between 10% and 30% in pollen-allergic patients in Europe.73 In 1 study, over 50% of patients sensitized to profilins experienced oral allergy symptoms with plant-derived foods.73 However, clinical pollen-food allergy in profilin-sensitized patients may be independent of the level of specific IgE.74,75 The first profilin identified was Bet v 2, an allergen in birch pollen. IgE antibodies in birch pollen-food–allergic individuals cross-react with Bet v 2 homologous proteins from apple, pear, melon, carrot, celery, and potato (Table 1, 2, 5).28,76–78 Similarly, patients with allergies to grass pollen profilin may have OAS in response to eating peaches and apples that contain these profilin proteins.79 Patients who are sensitized to profilin tend to also be sensitized to mugwort and ragweed pollen in addition to birch and grass pollen.73 Profilin has been implicated in the mugwort-celery-spice syndrome and ragweed-melon allergy (Table 2, 3, 5).80,81 Fruit allergy to melon, watermelon, tomato, banana, pineapple, and orange may be considered a marker of profilin hypersensitivity (Table 5).73 Profilin sensitization in pollen-allergic individuals is common in southern Europe with prevalence rates of 6% in Spain’s Mediterranean coast,11 21% in Portugal,82 and 30% in Italy.73
Although exclusion diets have been successful in the treatment of simple food allergies in some adults (∼1/3),85 with reports of food allergies being eliminated after strict avoidance for 2 years,86,87 food avoidance does not seem to have a role in OAS because the latter is due to cross-reaction to pollen rather than food protein. Oral allergy syndrome tends to be perennial, perhaps due to continued exposure to the corresponding and cross-reacting aeroallergens.88 Moreover, peeling the suspect foods may not provide adequate protection because the flesh may contain the provocative allergen or become contaminated during handling. However, antihistamines have been reported useful when taken before eating raw fruits and vegetables.89
Allergens in OAS typically are labile and therefore heat sensitive. Cooking suspect food is therefore 1 potential solution.90 Steam cooking kiwi for 5 minutes at 100°C has been reported to increase tolerance of kiwi in kiwi-allergic children with OAS (Table 1).91 Industrial homogenization of kiwi involving a 4-step heating process of scalding for 5 minutes at 90°C, heat treatment for 15 seconds at 115°C, stabilization for 15 seconds at 110°C, and pasteurization for 21 minutes at 65°C was also shown to eliminate kiwi sensitivity.91 Other studies have demonstrated that thermal stability of allergenic proteins in kiwi is strongly dependent on the pH.92 The antigenicity of soybean products increases at 5 minutes of boiling and gradually decreases as the duration of boiling approaches 60 minutes.93 However, diagnostic accuracy is vital in this setting because those experiencing other types of food allergy may not be protected by this exercise. Thermal processing of fruits has not been uniformly effective in decreasing their allergenicity. The disulfide bond-stabilized structure of the LTP molecule makes these proteins extremely resistant to heat denaturation.64 In addition, many foods contain both heat-stable LTPs and heat-labile PR-10 proteins (Table 6), and therefore, whether or not heating the food will result in clinical resolution of symptoms depends on which protein the patient is allergic to. Component-resolved microarray immunoassay is promising in identifying specific IgE to individual allergens, but the low sensitivity of the assay limits its utility.94 Roasted peanuts are apparently more allergenic than raw peanuts (Table 1). Roasting raw peanuts at 55°C for 10 days was shown to increase the IgE-binding activity of 2 major peanut allergens Ara h 1 and Ara h 2 as compared with raw peanuts.95 Higher allergenicity was also demonstrated with commercially roasted peanuts as compared with raw and boiled peanuts.96 More recently, autoclaving roasted peanuts at 138°C for 15 and 30 minutes has been demonstrated to produce a significant decrease of IgE-binding capacity of peanut allergens, although further studies are needed to confirm the clinical relevance of these findings.97 Hazelnuts roasted at 140°C for 40 minutes have also been shown to cause OAS in certain hazelnut-allergic patients (Table 1).98 In addition, in a subset of patients, those with OAS-like symptoms but without an aeroallergen sensitization, IgE reactivity to Mal d 3, an LTP from apple, has been shown via radioallergosorbent testing to remain unchanged despite moderate (90°C, 20 minutes) thermal treatment.99 In addition, the nonspecific LTP, Pru av 3, in cherries has been shown to retain a much higher allergenic potency after thermal processing (Table 1).100 Recombinant cherry allergens were heated at increments of 20°C, 40°C, 70°C, and 100°C during CD spectroscopy.100 In this subset of patients, therefore, heating is ineffective for prophylaxis. In addition, consumption of cooked birch-related fruits by patients with birch pollen allergy and atopic dermatitis has been implicated in flaring eczema.101 In patients with birch pollen allergy and atopic dermatitis, cooked birch-related food allergens trigger a cellular response that is not dependent on IgE binding.101 Cooked birch-related food allergens lose the capacity to bind IgE but retain their ability to activate Bet v 1–specific T-cells as native proteins and trigger atopic dermatitis.101
Ideally, the specific allergens causing symptoms should be easily identified in any patient; however, this is not always feasible. Fruits and vegetables may contain more than 1 allergenic protein, often from different antigenically distinct families. Individual sensitization profiles to these proteins may also vary due to dietary habits and pollinoses in each geographical area.118 In northern and central Europe, allergic reactions to plant foods are associated with birch pollen allergens Bet v 1 homologs and profilins.3 In North America, important aeroallergens include birch, rye grass, Bermuda grass, and ragweed.119 In southern Europe, allergy to fruits of the Rosaceae family is attributed to grass pollen sensitization rather than to birch pollen.79 In the Mediterranean area, LTPs are dominant allergens, whereas LTP allergy is rarely reported in central and northern Europe.3,61 Olive and Salsola pollen are largely responsible for cross-sensitizations with foods in Mediterranean regions.3,61,120 In northern China, exposure to mugwort LTP Art v 3 has been implicated in causing peach allergy,121 whereas in southern Europe, peach allergy is attributed to primary sensitization to peach LTP Pru p 3.122 Geography greatly contributes to the diagnostic complexity of pollen-food syndrome.
For patients with symptoms related to nuts, more restrictive and cautious recommendations should be suggested to prevent potentially more serious or generalized hypersensitivity reactions. Similarly, allergy to peaches and other LTP food allergens, which have also been implicated in more severe reactions, should also raise the level of caution.12 Patients with allergic rhinitis and classic OAS to other fruits and vegetables can be reassured that their symptoms are not likely to progress to anaphylaxis. Understanding the pathogenesis, triggers, management, and prognosis of OAS can enable early intervention and potentially lessen the morbidity associated with the disease.
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